Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells
Human Cripto‐1 (CR‐1) plays an important role in regulating embryonic development while also regulating various stages of tumor progression. However, mechanisms that regulate CR‐1 expression during embryogenesis and tumorigenesis are still not well defined. In the present study, we investigated the...
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| Veröffentlicht in: | Journal of cellular physiology 2013-06, Vol.228 (6), p.1174-1188 |
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| creator | Bianco, Caterina Castro, Nadia P. Baraty, Christina Rollman, Kelly Held, Natalie Rangel, Maria Cristina Karasawa, Hideaki Gonzales, Monica Strizzi, Luigi Salomon, David S. |
| description | Human Cripto‐1 (CR‐1) plays an important role in regulating embryonic development while also regulating various stages of tumor progression. However, mechanisms that regulate CR‐1 expression during embryogenesis and tumorigenesis are still not well defined. In the present study, we investigated the effects of two nuclear receptors, liver receptor homolog (LRH)‐1 and germ cell nuclear factor receptor (GCNF) and epigenetic modifications on CR‐1 gene expression in NTERA‐2 human embryonal carcinoma cells and in breast cancer cells. CR‐1 expression in NTERA‐2 cells was positively regulated by LRH‐1 through direct binding to a DR0 element within the CR‐1 promoter, while GCNF strongly suppressed CR‐1 expression in these cells. In addition, the CR‐1 promoter was unmethylated in NTERA‐2 cells, while T47D, ZR75‐1, and MCF7 breast cancer cells showed high levels of CR‐1 promoter methylation and low CR‐1 mRNA and protein expression. Treatment of breast cancer cells with a demethylating agent and histone deacetylase inhibitors reduced methylation of the CR‐1 promoter and reactivated CR‐1 mRNA and protein expression in these cells, promoting migration and invasion of breast cancer cells. Analysis of a breast cancer tissue array revealed that CR‐1 was highly expressed in the majority of human breast tumors, suggesting that CR‐1 expression in breast cancer cell lines might not be representative of in vivo expression. Collectively, these findings offer some insight into the transcriptional regulation of CR‐1 gene expression and its critical role in the pathogenesis of human cancer. J. Cell. Physiol. 228: 1174–1188, 2013. © 2012 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jcp.24271 |
| format | Article |
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However, mechanisms that regulate CR‐1 expression during embryogenesis and tumorigenesis are still not well defined. In the present study, we investigated the effects of two nuclear receptors, liver receptor homolog (LRH)‐1 and germ cell nuclear factor receptor (GCNF) and epigenetic modifications on CR‐1 gene expression in NTERA‐2 human embryonal carcinoma cells and in breast cancer cells. CR‐1 expression in NTERA‐2 cells was positively regulated by LRH‐1 through direct binding to a DR0 element within the CR‐1 promoter, while GCNF strongly suppressed CR‐1 expression in these cells. In addition, the CR‐1 promoter was unmethylated in NTERA‐2 cells, while T47D, ZR75‐1, and MCF7 breast cancer cells showed high levels of CR‐1 promoter methylation and low CR‐1 mRNA and protein expression. Treatment of breast cancer cells with a demethylating agent and histone deacetylase inhibitors reduced methylation of the CR‐1 promoter and reactivated CR‐1 mRNA and protein expression in these cells, promoting migration and invasion of breast cancer cells. Analysis of a breast cancer tissue array revealed that CR‐1 was highly expressed in the majority of human breast tumors, suggesting that CR‐1 expression in breast cancer cell lines might not be representative of in vivo expression. Collectively, these findings offer some insight into the transcriptional regulation of CR‐1 gene expression and its critical role in the pathogenesis of human cancer. J. Cell. Physiol. 228: 1174–1188, 2013. © 2012 Wiley Periodicals, Inc.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.24271</identifier><identifier>PMID: 23129342</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Azacitidine - analogs & derivatives ; Azacitidine - pharmacology ; Binding Sites ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Carcinoma, Ductal, Breast - genetics ; Carcinoma, Ductal, Breast - metabolism ; Carcinoma, Ductal, Breast - pathology ; Carcinoma, Embryonal - genetics ; Carcinoma, Embryonal - metabolism ; Carcinoma, Embryonal - pathology ; Cell Movement ; Decitabine ; DNA Methylation - drug effects ; DNA Modification Methylases - antagonists & inhibitors ; DNA Modification Methylases - metabolism ; Dose-Response Relationship, Drug ; Embryonal Carcinoma Stem Cells - metabolism ; Embryonal Carcinoma Stem Cells - pathology ; Embryonic growth stage ; Female ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; GPI-Linked Proteins - genetics ; GPI-Linked Proteins - metabolism ; Histone Deacetylase Inhibitors - pharmacology ; Humans ; Hydroxamic Acids - pharmacology ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Luciferases - biosynthesis ; Luciferases - genetics ; MCF-7 Cells ; Methylation ; Neoplasm Invasiveness ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Nuclear Receptor Subfamily 6, Group A, Member 1 - genetics ; Nuclear Receptor Subfamily 6, Group A, Member 1 - metabolism ; Promoter Regions, Genetic ; Receptors, Cytoplasmic and Nuclear - genetics ; Receptors, Cytoplasmic and Nuclear - metabolism ; RNA Interference ; RNA, Messenger - metabolism ; Time Factors ; Tissue Array Analysis ; Transcription, Genetic ; Transfection ; Tretinoin - pharmacology ; Valproic Acid - pharmacology</subject><ispartof>Journal of cellular physiology, 2013-06, Vol.228 (6), p.1174-1188</ispartof><rights>Copyright © 2012 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5141-849cbd063a5b625769ec503eca2fff8bb2dbab7ccec02f9e6791e57669d63cc83</citedby><cites>FETCH-LOGICAL-c5141-849cbd063a5b625769ec503eca2fff8bb2dbab7ccec02f9e6791e57669d63cc83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.24271$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.24271$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23129342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bianco, Caterina</creatorcontrib><creatorcontrib>Castro, Nadia P.</creatorcontrib><creatorcontrib>Baraty, Christina</creatorcontrib><creatorcontrib>Rollman, Kelly</creatorcontrib><creatorcontrib>Held, Natalie</creatorcontrib><creatorcontrib>Rangel, Maria Cristina</creatorcontrib><creatorcontrib>Karasawa, Hideaki</creatorcontrib><creatorcontrib>Gonzales, Monica</creatorcontrib><creatorcontrib>Strizzi, Luigi</creatorcontrib><creatorcontrib>Salomon, David S.</creatorcontrib><title>Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells</title><title>Journal of cellular physiology</title><addtitle>J. Cell. Physiol</addtitle><description>Human Cripto‐1 (CR‐1) plays an important role in regulating embryonic development while also regulating various stages of tumor progression. However, mechanisms that regulate CR‐1 expression during embryogenesis and tumorigenesis are still not well defined. In the present study, we investigated the effects of two nuclear receptors, liver receptor homolog (LRH)‐1 and germ cell nuclear factor receptor (GCNF) and epigenetic modifications on CR‐1 gene expression in NTERA‐2 human embryonal carcinoma cells and in breast cancer cells. CR‐1 expression in NTERA‐2 cells was positively regulated by LRH‐1 through direct binding to a DR0 element within the CR‐1 promoter, while GCNF strongly suppressed CR‐1 expression in these cells. In addition, the CR‐1 promoter was unmethylated in NTERA‐2 cells, while T47D, ZR75‐1, and MCF7 breast cancer cells showed high levels of CR‐1 promoter methylation and low CR‐1 mRNA and protein expression. Treatment of breast cancer cells with a demethylating agent and histone deacetylase inhibitors reduced methylation of the CR‐1 promoter and reactivated CR‐1 mRNA and protein expression in these cells, promoting migration and invasion of breast cancer cells. Analysis of a breast cancer tissue array revealed that CR‐1 was highly expressed in the majority of human breast tumors, suggesting that CR‐1 expression in breast cancer cell lines might not be representative of in vivo expression. Collectively, these findings offer some insight into the transcriptional regulation of CR‐1 gene expression and its critical role in the pathogenesis of human cancer. J. Cell. Physiol. 228: 1174–1188, 2013. © 2012 Wiley Periodicals, Inc.</description><subject>Azacitidine - analogs & derivatives</subject><subject>Azacitidine - pharmacology</subject><subject>Binding Sites</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinoma, Ductal, Breast - genetics</subject><subject>Carcinoma, Ductal, Breast - metabolism</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Carcinoma, Embryonal - genetics</subject><subject>Carcinoma, Embryonal - metabolism</subject><subject>Carcinoma, Embryonal - pathology</subject><subject>Cell Movement</subject><subject>Decitabine</subject><subject>DNA Methylation - drug effects</subject><subject>DNA Modification Methylases - antagonists & inhibitors</subject><subject>DNA Modification Methylases - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Embryonal Carcinoma Stem Cells - metabolism</subject><subject>Embryonal Carcinoma Stem Cells - pathology</subject><subject>Embryonic growth stage</subject><subject>Female</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Reporter</subject><subject>GPI-Linked Proteins - genetics</subject><subject>GPI-Linked Proteins - metabolism</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Luciferases - biosynthesis</subject><subject>Luciferases - genetics</subject><subject>MCF-7 Cells</subject><subject>Methylation</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Nuclear Receptor Subfamily 6, Group A, Member 1 - genetics</subject><subject>Nuclear Receptor Subfamily 6, Group A, Member 1 - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Receptors, Cytoplasmic and Nuclear - genetics</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><subject>Tissue Array Analysis</subject><subject>Transcription, Genetic</subject><subject>Transfection</subject><subject>Tretinoin - pharmacology</subject><subject>Valproic Acid - pharmacology</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAURi0EokNhwQsgS2xgkdY_iR1vkKpAW1ApVQViadmem06GJA52As2eB8fTmY4AiZUX37lH1_dD6DklR5QQdrx2wxHLmaQP0IISJbNcFOwhWqSMZqrI6QF6EuOaEKIU54_RAeOUKZ6zBfp1DTdTa8bG99jXeDV1psdVaIbRZxTD7RAgxk1oZ9xPrgUTcAAHKQ8Rm36J316e4CH4zo8QcAfjat7pmn6ng86G2femveNtABNH7Ezv0oCDto1P0aPatBGe7d5D9OX03efqPLv4dPa-OrnIXEFzmpW5cnZJBDeFFayQQoErCAdnWF3XpbVsaY2VzoEjrFYgpKKQMKGWgjtX8kP0ZusdJtvB0kE_BtPqITSdCbP2ptF_J32z0jf-h-aF5IwWSfBqJwj--wRx1F0TN18wPfgpappzxXjJmUzoy3_QtZ9COkKiOJW5KHPCE_V6S7ngYwxQ75ehRG-61albfddtYl_8uf2evC8zAcdb4GfTwvx_k_5QXd0rs-1EE0e43U-Y8E0LyWWhv16eaVFdfZTX55U-5b8B8qHAEw</recordid><startdate>201306</startdate><enddate>201306</enddate><creator>Bianco, Caterina</creator><creator>Castro, Nadia P.</creator><creator>Baraty, Christina</creator><creator>Rollman, Kelly</creator><creator>Held, Natalie</creator><creator>Rangel, Maria Cristina</creator><creator>Karasawa, Hideaki</creator><creator>Gonzales, Monica</creator><creator>Strizzi, Luigi</creator><creator>Salomon, David S.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7TM</scope><scope>5PM</scope></search><sort><creationdate>201306</creationdate><title>Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells</title><author>Bianco, Caterina ; Castro, Nadia P. ; Baraty, Christina ; Rollman, Kelly ; Held, Natalie ; Rangel, Maria Cristina ; Karasawa, Hideaki ; Gonzales, Monica ; Strizzi, Luigi ; Salomon, David S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5141-849cbd063a5b625769ec503eca2fff8bb2dbab7ccec02f9e6791e57669d63cc83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Azacitidine - analogs & derivatives</topic><topic>Azacitidine - pharmacology</topic><topic>Binding Sites</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinoma, Ductal, Breast - genetics</topic><topic>Carcinoma, Ductal, Breast - metabolism</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Carcinoma, Embryonal - genetics</topic><topic>Carcinoma, Embryonal - metabolism</topic><topic>Carcinoma, Embryonal - pathology</topic><topic>Cell Movement</topic><topic>Decitabine</topic><topic>DNA Methylation - drug effects</topic><topic>DNA Modification Methylases - antagonists & inhibitors</topic><topic>DNA Modification Methylases - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Embryonal Carcinoma Stem Cells - metabolism</topic><topic>Embryonal Carcinoma Stem Cells - pathology</topic><topic>Embryonic growth stage</topic><topic>Female</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Reporter</topic><topic>GPI-Linked Proteins - genetics</topic><topic>GPI-Linked Proteins - metabolism</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Luciferases - biosynthesis</topic><topic>Luciferases - genetics</topic><topic>MCF-7 Cells</topic><topic>Methylation</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Nuclear Receptor Subfamily 6, Group A, Member 1 - genetics</topic><topic>Nuclear Receptor Subfamily 6, Group A, Member 1 - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Receptors, Cytoplasmic and Nuclear - genetics</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><topic>Tissue Array Analysis</topic><topic>Transcription, Genetic</topic><topic>Transfection</topic><topic>Tretinoin - pharmacology</topic><topic>Valproic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bianco, Caterina</creatorcontrib><creatorcontrib>Castro, Nadia P.</creatorcontrib><creatorcontrib>Baraty, Christina</creatorcontrib><creatorcontrib>Rollman, Kelly</creatorcontrib><creatorcontrib>Held, Natalie</creatorcontrib><creatorcontrib>Rangel, Maria Cristina</creatorcontrib><creatorcontrib>Karasawa, Hideaki</creatorcontrib><creatorcontrib>Gonzales, Monica</creatorcontrib><creatorcontrib>Strizzi, Luigi</creatorcontrib><creatorcontrib>Salomon, David S.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bianco, Caterina</au><au>Castro, Nadia P.</au><au>Baraty, Christina</au><au>Rollman, Kelly</au><au>Held, Natalie</au><au>Rangel, Maria Cristina</au><au>Karasawa, Hideaki</au><au>Gonzales, Monica</au><au>Strizzi, Luigi</au><au>Salomon, David S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J. Cell. Physiol</addtitle><date>2013-06</date><risdate>2013</risdate><volume>228</volume><issue>6</issue><spage>1174</spage><epage>1188</epage><pages>1174-1188</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Human Cripto‐1 (CR‐1) plays an important role in regulating embryonic development while also regulating various stages of tumor progression. However, mechanisms that regulate CR‐1 expression during embryogenesis and tumorigenesis are still not well defined. In the present study, we investigated the effects of two nuclear receptors, liver receptor homolog (LRH)‐1 and germ cell nuclear factor receptor (GCNF) and epigenetic modifications on CR‐1 gene expression in NTERA‐2 human embryonal carcinoma cells and in breast cancer cells. CR‐1 expression in NTERA‐2 cells was positively regulated by LRH‐1 through direct binding to a DR0 element within the CR‐1 promoter, while GCNF strongly suppressed CR‐1 expression in these cells. In addition, the CR‐1 promoter was unmethylated in NTERA‐2 cells, while T47D, ZR75‐1, and MCF7 breast cancer cells showed high levels of CR‐1 promoter methylation and low CR‐1 mRNA and protein expression. Treatment of breast cancer cells with a demethylating agent and histone deacetylase inhibitors reduced methylation of the CR‐1 promoter and reactivated CR‐1 mRNA and protein expression in these cells, promoting migration and invasion of breast cancer cells. Analysis of a breast cancer tissue array revealed that CR‐1 was highly expressed in the majority of human breast tumors, suggesting that CR‐1 expression in breast cancer cell lines might not be representative of in vivo expression. Collectively, these findings offer some insight into the transcriptional regulation of CR‐1 gene expression and its critical role in the pathogenesis of human cancer. J. Cell. Physiol. 228: 1174–1188, 2013. © 2012 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>23129342</pmid><doi>10.1002/jcp.24271</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Azacitidine - analogs & derivatives Azacitidine - pharmacology Binding Sites Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Carcinoma, Ductal, Breast - genetics Carcinoma, Ductal, Breast - metabolism Carcinoma, Ductal, Breast - pathology Carcinoma, Embryonal - genetics Carcinoma, Embryonal - metabolism Carcinoma, Embryonal - pathology Cell Movement Decitabine DNA Methylation - drug effects DNA Modification Methylases - antagonists & inhibitors DNA Modification Methylases - metabolism Dose-Response Relationship, Drug Embryonal Carcinoma Stem Cells - metabolism Embryonal Carcinoma Stem Cells - pathology Embryonic growth stage Female Gene Expression Regulation, Developmental Gene Expression Regulation, Neoplastic Genes, Reporter GPI-Linked Proteins - genetics GPI-Linked Proteins - metabolism Histone Deacetylase Inhibitors - pharmacology Humans Hydroxamic Acids - pharmacology Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Luciferases - biosynthesis Luciferases - genetics MCF-7 Cells Methylation Neoplasm Invasiveness Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Nuclear Receptor Subfamily 6, Group A, Member 1 - genetics Nuclear Receptor Subfamily 6, Group A, Member 1 - metabolism Promoter Regions, Genetic Receptors, Cytoplasmic and Nuclear - genetics Receptors, Cytoplasmic and Nuclear - metabolism RNA Interference RNA, Messenger - metabolism Time Factors Tissue Array Analysis Transcription, Genetic Transfection Tretinoin - pharmacology Valproic Acid - pharmacology |
| title | Regulation of human Cripto-1 expression by nuclear receptors and DNA promoter methylation in human embryonal and breast cancer cells |
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